Cited by 33Viral Infections and Immunology ResearchCardiac Fibrosis and RemodelingAdipokines, Inflammation, and Metabolic Diseases

Adiponectin Replacement Therapy Attenuates Myocardial Damage in Leptin-deficient Mice with Viral Myocarditis

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Takahashi, T, Saegusa, S, Sumino, H, Nakahashi, T, Iwai, K, Morimoto, S, Kanda, T·2005·Journal of International Medical Research

Abstract

The effects of adiponectin replacement therapy on myocardial damage were studied in leptin-deficient (OB) mice with acute viral myocarditis. Encephalomyocarditis virus was injected intraperitoneally into OB and wild-type (WT) mice. One subgroup of OB mice received no intervention and another subgroup received daily adiponectin replacement, simultaneously with viral inoculation. Differences in heart weight, cardiac histological score, numbers of infiltrating or apoptotic cells in the myocardium and the immunoreactivity of adiponectin receptors in myocytes were determined. The reactivity of adiponectin receptor 1 in myocytes from OB mice on day 4 and day 8 after viral inoculation was significantly decreased compared with that in myocytes from WT mice; the OB mice also had elevated cardiac weights and severe inflammatory myocardial damage. Adiponectin replacement in OB mice inhibited the development of severe myocarditis by augmenting myocyte adiponectin receptor 1 reactivity. Exogenously administered adiponectin may inhibit the progression of viral myocarditis through binding to the adiponectin receptor 1 in leptin-deficient conditions.

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Crossref · 10.1177/147323000503300208

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15 of 15 references verified0 citation errors · 0 not checkable

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  • Myocardial necrosis in obese mice with viral myocarditis was attenuated upon endogenous cardiac induction of adiponectin expression, suggesting this may represent a compensatory protective response.

    “Furthermore, myocardial necrosis in obese mice with viral myocarditis was attenuated upon endogenous cardiac induction of adiponectin expression, suggesting this may represent a compensatory protective response (167, 338, 340).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [338]

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Authors
Takahashi, T., Saegusa, S., Sumino, H., Nakahashi, T., Iwai, K., Morimoto, S., & Kanda, T.
Affiliations
  • Kanazawa Medical University (JP)
  • Gunma University (JP)
Corresponding author
Kanda, T
Venue
Journal of International Medical Research
Published
2005-03
Volume
33
Issue
2
Pages
207-214
ISSN
  • 0300-0605 (ISSN-L)
  • 1473-2300
OpenAlex
W2011591230
Cited by
33
References
14
Citations by year
2026: 1 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 1
FWCI
2.51
Type
journal article
Language
en
Open access
Locations
  • Journal of International Medical Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Kanazawa Medical University (H2004-7)
  • Promotion and Mutual Aid Corporation for Private Schools of Japan
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
leptin deficiency, viral myocarditis, encephalomyocarditis virus, myocardial injury, AdipoR1, cardiac inflammation, cardiomyocyte apoptosis, cardiac hypertrophy, ob/ob mice
MeSH terms
Animals, Body Weight, Encephalomyocarditis virus, Heart, Mice, Inbred C57BL, Mice, Transgenic, Myocarditis, Myocardium, Organ Size, Protein Binding, Receptors, Cell Surface, Time Factors, Genetic Therapy, Apoptosis, Disease Progression, Leptin, Muscle Cells, Intercellular Signaling Peptides and Proteins, Mice, Adiponectin, Receptors, Leptin, Receptors, Adiponectin

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